The deregulated activity of PI3K, AKT, mTORC1/mTORC2, or their corresponding downstream substrates can be the result of genetic alterations, of which the most frequent are the overexpressing/activating mutations in genes encoding RTKs (e.g., EGFR and ERBB2 genes), PI3K subunits (PI3KCA, PI3KCB, PI3KCG, and PI3KCD genes), or AKT isoforms (AKT1, AKT2, or AKT3 genes); and deletions or inactivating mutations in tumor suppressor genes (e.g., PTEN gene) [22,42,43,44,45]. The gene discussed is AKT1; the disease is neoplasm.